DESCRIPTION (Adapted from investigator's abstract) The hypothesis is that the rise in intraocular pressure seen in steroid-response glaucoma is due to a decrease in tPA activity in the extracellular space of the trabecular meshwork (TM). Enzymes such as tPA and plasmin (which can be activated by tPA) can digest extracellular matrix components such as fibronectin, laminin, and elastin, which may help clear TM channels. In some cultured cells, corticosteroids have been shown to decrease the production of tPA or to stimulate the secretion of plasminogen activator inhibitor-1 (PAI-1). In this project, the relationship between the levels of tPA and PAI-1 and the resulting decrease in fibrinolytic activity in steroid-treated TM organ cultures will be investigated using fibrin overlay of TM cultures, zymography and ELISA testing of culture supernatants, and immunohistology of the cultured tissues.